Researchers have identified a specific group of neurons in the amygdala that plays a central role in anxiety and social withdrawal. By restoring normal activity in this circuit, they reversed anxiety-related behaviors in mice. The findings point to a potential new target for treating emotional disorders.
The study, led by Juan Lerma at the Institute for Neurosciences in Elche, Spain, focused on the basolateral amygdala. Scientists used mice engineered to overexpress the Grik4 gene, which made certain neurons overly excitable and produced anxiety-like symptoms. Normalizing Grik4 activity in this region restored communication with inhibitory neurons in the centrolateral amygdala. This single adjustment reversed both anxiety and social deficit behaviors, according to first author Álvaro García. The same intervention also reduced anxiety in wild-type mice that naturally showed elevated levels. Object recognition memory deficits remained unchanged, suggesting other brain areas are involved in some symptoms. The work was published in iScience and funded by Spanish research agencies including the State Research Agency and the Generalitat Valenciana.
